Step 1 - Neuro 2

denniskwinn's version from 2015-04-25 16:11


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Anterior spinal artery deficitmedial medullary syndrome - contralateral hemiparesis (lower extremities), medial leminscus (↓ contralateral proprioception), ipsilateral paralysis of hypoglossal nerve
PICA deficit(lateral medullary syndrome, wallenberg’s) contralateral loss of pain and temperature, ipsilateral dysphagia, hoarsness, ↓ gag reflex, vertigo, diplopia, nystagymus, vomiting, ipsilateral horner’s, ipsilateral facial pain and temperature, trigeminal nucleus, ipsilateral ataxia
AICA deficit(lateral inferior pontine syndrome) - Ipsilateral facial paralysis, ipsilateral cochlear ucleus, vestibular (nystagmus), ipsilateral facial pain and temperature, ipsilateral dystaxia (MCP, ICP)
Posterior cerebral artery deficitcontralateral homonymous hemianopia w/ macular sparing; supplie occipital cortex
Middle cerebral artery deficitContralateral face and arm paralysis and sensory loss, aphasia (dominant sphere), left-sided neglect
Anterior cerebral artery defectsupplies medial surface of the brain, leg-foot area of motor and sensory cortices
Anterior cerebral artery deficitsupplies medial surface of the brain, leg-foot area of motor and sensory cortices
Anterior communicating artery deficitmost common site of circle of Willis aneurysm; lesions may causes visual field defects
PCA deficitcommon area of aneurysm, causes CNIII palsy
Lateral striate deficitDivisions of MCA - supply internal capsule, caudate, putamen, globus pallidus. “arteries of stroke”; infarct of the posterior limb of the internal capsule causes pure motor hemiparesis
Watershed zonesbetween ACA/MCA, PCA/MCA. Damage in severe hypotension→ upper leg/upper arm weakness, defects in higher order visual processing
Basilar artery defectinfarct causes “locked-in syndrome” (CN III is typically intact)
Damage of stroke of anterior circlegeneral sensory and motor dysfunction, aphasia
Damage from stroke of posterior circlecranial nerve deficits (vertigo, visual deficits), coma, cerebellar deficits (ataxia) dominant hemisphere (ataxia), nondominant (neglect)
Berry Aneurysmsoccur at bifurcations in circle of willis (most common ACA) 2. Rupture leads to hemorrhagic stroke/SAH 3. Assoc w/ adult polycystic kidney disease, Ehlers-Danlos syndrome and marfan’s. 4. Risk factors: advanced age, HTN, smoking, race (higher risk in blacks)
Charcol-Bouchard microaneurysmsassociated with chronic hypertension, affects small vessels (in basal ganglia, thalamus)
Epidural hematoma CTshows biconvex disk - not crossing suture lines - can cross falx, tentorium
Epidural hematomarupture of middle meningeal artery - often secondary to fracture of temporal bone. Lucid interval. Rapid expansion under systemic arterial pressure→ transtentorial herniation. CNIII palsy
Subdural hematoma imagingcrescent-shaped hemorrhage that crosses suture lines, Gyri are preserved since pressure is distributed equally. Cannot cross falx, tentorium
Subdural hematomarupture of bridging veins - slow venous bleeding. Delayed onset of symptoms. Seen in elderly individuals, alcoholics, blunt trauma, shaken baby
SAH1. rupture of an aneurysm or an AVM 2. patients complain of “worst headache of my life” 3. Bloody or yellow spinal tap 4. 2-3 days afterward there is a risk of vaspospasm due to blood breakdown products which irritate vessels (treat w/Ca channel blockers)
Parenchymal hematomacaused by HTN, amyloid angiopathy. Lobar strokes all over the brain. DM and tumor. Typically occurs in basal ganglia and internal capsule.
Most vulnerable parts to ischemic brainhippocampus, neocortex, cerebellum, watershed areas
Irreversible neuronal injury ( red neurons (12-48 hours), necrosis+neutrophils (24-72 hours), macrophages (3-5 days), reactive gliosis+ vasc proliferation (1-2 weeks), glial scar (> 2 weeks)
Atherosclerosisthrombi lead to ischemic stroke with subsequent necrosis (red neurons) - forms cystic cavity w/reactive gliosis
Hemorrhagic strokesintracerebral bleeding, often due to aneurysm rupture - may be secondary to ischmic stroke following reperfusion (↑ vessel fragility)
Ischemic strokeemboli block large vessels 2. Atrial fibrillation, carotid dissection, PFO, endocarditis, lacunar strokes block small vessels - secondary to HTN 3. Tx w/ tPA for 3 hours
Transient Ischemic attackbrief, reversible episode of neurologic dysfunction due to focal ischemia. Typically sx last for <24 hours
Stroke imagingbright on diffusion weighted MRI from 3-30 min post stroke to 10 days. Dark on CT for 24 hours
Lateral ventricle → 3rd viaforamen of Monro
3rd ventricle → 4th viacerebral aqueduct
4th ventricle → subarachnoid space viaForamina of Luschka (lateral), Foramen of Magendie (medial)
Normal pressure hydrocephaluswet, wobbly and wacky - does not result in ↑ subarachnoid space volume. Expansion of ventricles distorts the fibers of the corona radiata and leads to the clinical triad of dementia, ataxia and urinary incontinence ( a reversible cause of dementia in the elderly)
Communicating hydrocephalus↓CSF absorption by arachnoid villi →↑ICP, papilledema and herniation
Obstructive (noncommunicating) hydrocephaluscaused by a structural blockage of CSF circulation within the ventricular system (e.g. Stenosis of the aqueduct of Sylvius)
Hydrocephalus ex vacuoAppearance of ↑ CSF in atrophy (Alzheimer’s disease, advanced HIV, Pick’s disease) - Intracranial pressure is normal: triad is not seen
Lumbar puncture layers punctured (7)1. Skin/superficial fascia 2. Ligamets (supraspinous, interspinous, ligamentum flavum) 3. Epidural space 4. Dura Mater 5. Subdural space 6. Arachnoid 7. Subarachnoid space (CSF)
Ascending tractssynapse then cross
Dorsal column tract functionmedial lemniscal pathway (ascending pressure, vibration, touch and proprioceptive sensation)
Dorsal column 1st order neuronSensory nerve ending→DRG cell body→spinal cord ascend IL dorsal column
Dorsal column synapse 1IL nucleus cuneatus or gracilis (medulla)
Dorsal column 2nd order neurondecussates in medulla→ascends contralaterally in medial lemniscus
Dorsal column synapse 2VPL(ventral posterolateral nucleus) of thalamus
Dorsal column third order neuronSensory cortex
Spinothalamic tract functionascending pain and temperature sensation
Spinothalamic 1st order neuronSensory nerve ending (A-delta and C fibers) (cell body in DRG)→enters spinal cord
Spinothalamic tract synapse 1IL gray matter in spinal cord
Spinothalamic 2nd order neuronDecussates at anterior white commissure→ascends contralaterally
Spinothalamic synapse 2VPL of thalamus
Spinothalamic 3rd order neuronSensory cortex
Lateral corticospinal tract functiondescending voluntary movement of contralateral limbs
Lateral corticospinal tract 1st order neuronUMN (cell body in primary motor cortex)→descends IL (through internal capsuls) until decussating at caudal medulla (pyramidal decussation)→ descends contralaterally
Lateral corticospinal tract synapse 1cell body of anterior horn of spinal cord
Lateral corticospinal tract second order neuronLMN (leaves spinal cord)
Lateral corticospinal tract synapse 2NM junction
UMN disease signs( weakness, hyperreflexia, increased tone, +babinski, +spastic paralysis, +clasp knife spasticity
LMN lesion signs( 5)1.weakness, 2. atrophy, 3. fasciculation (twitching) , 4. hyporeflexia, 5. low tone
Draw out the lesions on page 407draw draw draw
PoliomyelitisCaused by poliovirus, which is trasmitted by fecal-oral route. Replicates in oropharvnx and SI before spreading through the bloodstream to CNS where it leads to the destruction of cells in the anterior horn of the spinal cord, leading to LMN destruction.
Polio sxMalaise, headache, fever, nausea, abdominal pain, sore throat. Signs of LMN lesions - muscle weakness and atrophy, fasciculations, fibrillation, hyporeflexia
Polio findingsCSF w/lymphocytic pleocytosis w/slight elevation of protein (w/no change in CSF glucose). Virus recovered from stool or throat.
Werdnig-Hoffman disease (6)1.aka infantile spinal muscular atrophy. 2.Autosomal-recessive inheritance; 3.presents at birth as “floppy baby”, 4.tongue fasciculations, median age of death 7 months. 5. Asso w/degeneration of anterior horns, 6.LMN only
Amylotrophic lateral sclerosis (1. Assoc with LMN and UMN signs 2. No sensory, cognitive or oculomotor deficits. 3. Can be caused by defect in superoxide dismutase, betel nut ingestion. 4. Commonly presents as fasciculations. 5. Aka Lou Gehrig’s disease
Tabes dorsalis (1. Degenerations of dorsal columns and dorsal roots due to tertiary syphilis. 2. Impaired proprioception and locomotor ataxia 3. Assoc w/ Charcot’s joints, shooting pain. Argyll robertson pupils, absence of DTRs, positive romberg and sensory ataxia
Argyll robertson pupilsaka prostitute pupils - reactive to accomodation, but not to light
Romberg testthe subject stands with feet together, eyes open and hands by the sides. Then the subject closes the eyes while the examiner observes for a full minute.
Friedreich’s ataxia1. Autosomal recessive trinucleotide repeat disorder 2. impairment in mitochondrial functioning, 2. Staggering gait, frequent falling, nystagmus, dysarthria, pes cavus, hammer toes, hypertrophic cardiomyopathy (cause of death) 4. Presents in childhood with kyphoscoliosis.
Brown - Sequard syndrome1. Ipsilateral UMN signs below hemisection lesion (corticospinal tract) of spinal cord 2. IL loss of tactile, vibration proprioception sense (dorsal column) below lesion 3. CL pain and temp loss below lesion ( spinothalamic) 4. IL loss of all sensation at level of lesion 5. LMN signs at level of lesion. 6. If lesion above T1 = Horner’s syndrome
Horner’s syndromesympathectomy of face 1. Ptosis 2. Anhidrosis 3. Miosis - assoc w/ lesion of spinal cord above T1
3-neuron oculosympathetic pathways1. project from hypothalamus to interomediolateral column of spinal cord, then to the superior cervical (sympathetics) ganglion and finally to the pupil. 2. Interruption of any of these results in Horner’s
C2 dermatomeposterior half of a skull "cap."
C3 dermatome high lurtleneck shirt.
C4 dermatomelow-collar shirt.
T4 dermatomeat the nipple.
T7 dermatomeat the xiphoid process.
T1O dermatomeat the umibilicus (important for early appendicitis pain referral).
L1 dermatome at the inguinal ligament.
L4 dermatome includes the kneecaps.
S2, S3, S4 dermatome erection and sensation of penile and anal zones.
Diaphragm and gallbladder referred painright shoulder via phrenic nerve
Muscle spindle monitormuscle length
Golgi tendon monitormuscle tension
Muscle spindle controlin parallel with extrafusal muscle - - Muscle stretch →intrafusal stretch→stimulates alpha motor neuron→reflex muscle (extrafusal contraction).
Golgi tendon controlperpendicular to intrafusal muscle Ib inhibitory feedback to alpha motor neurons
Gamma loopCNS stimulates gamma motor neuron → intrafusal contraction at central part of muscle spindle → ↑ sensitivity of reflex arc - can be influenced by the brain.
Biceps ReflexC5 nerve root
Triceps ReflecC7 nerve root
Patella Reflex L4 nerve root
Achilles reflexSI nerve root
Babinski reflexdorsiflexion of the big toe and fanning of other toes; sign of UMN lesion, but normal reflex in 1st year of life.
Moro reflex "hang on for life" reflex —abduct/extend limbs when startled, and then draw together - primitive reflex - usually disappear within first year of life, may reappear with frontal lobe lesion
Rooting reflexmovement of head toward one side if cheek or mouth is stroked (nipple seeking) - primitive reflex - usually disappear within first year of life, may reappear with frontal lobe lesion
Sucking reflexsucking response when roof of mouth is touched - primitive reflex - usually disappear within first year of life, may reappear with frontal lobe lesion
Palmar and plantar reflexescurling of fingers/toes if palms of hands/feel arc stroked -primitive reflex - usually disappear within first year of life, may reappear with frontal lobe lesion
Pineal gland melatonin secretion, circadian rhythms.
Superior colliciiliconjugate vertical gaze center.
Inferior eolliculiauditory.
Parinaud syndromeparalysis of conjugale vertical gaze due to lesion in superior colliciili (e.g.,pinealoma).
Cranial nerve nucleilocated in tegmentum portion of brain stem (b/w dorsal and ventral portions 2. Lateral nuclei are sensory Medial are motor 3. Midbrain III,IV, 4. Pons - V, VI, VII, VIII 5. Medulla IX, X, XI, XII
Corneal reflexafferent V1 ophthalmic (nasociliary branch: levator palpebrae), efferent VII (temporal branch: obicularis oculi)
Lacrimation reflexafferent V1, efferent VII (doesn’t stop emotional crying)
Jaw jerk reflexafferent V3 (sensory-muscle spindle of masseter) efferent V3 (motor of masseter)
Pupillary reflexAfferent II, Efferent III
Gag reflexafferent IX, efferent IX and X
Nucleus solitarusVagal nucleus - visceral sensory information (taste, baroreceptors, gut distention) - VII, IX, X
Nucleus ambiguusVagal nucleus - motor innervation of pharynx, larynx and upper esophagus (swallowing, palate elevation) - IX, X, XI
Nucleus dorsal motor nucleussends autonomic (Parasympathetic) fibers to heart, lungs, upper GI
Nerves through Cribiform plateCN I
Passing through Optic canalCN II, ophthalmic artery, central retinal vein
Passing through Superior orbital fissureCN III, IV, V1, VI, ophtlamic vein, sympathetic fibers
Passing through foramen rotundumCN V2
Passing through foramen ovaleCNV3
Passing through foramen spinosummiddle meningeal artery
Passing through internal auditory meatusCNVII, VIII
Passing through jugular foramenCNIX, X, XI, jugular vein
Passing through foramen magnumspinal roots of CNXI, brain stem, vertebral arteries
Passing through cavernous sinusCNIII, IV, V1,V2 and VI and postganglionic sympathetic fibers en route to the orbit.
Cavernous sinus syndromeopthalmoplegia, ophthalmic and maxillary sensory loss - due to mass effect